In cats, fifteen platinum microelectrodes, 25 microns in diameter, will be implanted to measure local cerebral blood flow (1CBF) by hydrogen clearance, 02 availability (polarographically), and tissue edema (high frequency impedance). These electrodes will be used to assess the time course and to optimize and rationalize the theraputic interventions in focal ischemic injury following middle cerebral artery occlusion (MCAO). One hypothesis to be tested with this model is that barbiturate protection is greater than that of halothane because barbiturates do not disturb the vasoconstrictor responses in adjacent normal or poorly perfused brain, permitting better anastomotic flow into the occluded tissue. A second hypothesis is that brain edema propagates by compressing adjacent microcirculation, causing more ischemia, hypoxia, hyperosomolarity and tissue acidosis. The effect of therapies, including hyperventilation, vasopressors, barbiturates, hypothermia, osmotic agents, steroids, helium inhalation and increased Pao2 will be tested. Tissue C02 electrodes will be used to test a third hypothesis that ischemic tissue acidosts elevates Pco2 and thus total gas pressure above the bubble nucleation threshold causing or contributing to irreversible vascular obstructions. Ultrasound will be used to detect bubbles in focal and global ischemia. The role of inert gas in formation and growth of these bubbles will be assessed by N2 elimination with 02 and He breathing. The hypothesis that glucose loading worsens the ischemic damage by increasing cerebral lactic acidosis and consequent bubble formation will be tested. The time courses of 1CBF, Ptco2 and CSF pH will be determined in both the global and focal ischemia models.